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Persistent pain is a major public health issue—estimated to affect a quarter of the world's population. Public understanding of persistent pain is based on outdated biomedical models, laden with misconceptions that are contrary to best evidence. This understanding is a barrier to effective pain management. Thus, there have been calls for public health-based interventions to address these misconceptions. Previous pain-focussed public education campaigns have targeted pain beliefs and behaviours that are thought to promote recovery, such as staying active. However, prevailing pain-related misconceptions render many of these approaches counter-intuitive, at best. Pain Science Education improves understanding of ‘how pain works’ and has been demonstrated to improve pain and disability outcomes. Extending Pain Science Education beyond the clinic to the wider community seems warranted. Learning from previous back pain-focussed and other public health educational campaigns could optimise the potential benefit of such a Pain Science Education campaign. Pain Science Education-grounded campaigns have been delivered in Australia and the UK and show promise, but robust evaluations are needed before any firm conclusions on their population impact can be made. Several challenges exist going forward. Not least is the need to ensure all stakeholders are involved in the development and implementation of Pain Science Education public messaging campaigns. Furthermore, it is crucial that campaigns are undertaken through a health equity lens, incorporating underrepresented communities to ensure that any intervention does not widen existing health inequalities associated with persistent pain. Perspective: Public misconceptions about pain are a significant public health challenge and a viable intervention target to reduce the personal, social, and economic burden of persistent pain. Adaptation of Pain Science Education, which improves misconceptions in a clinical setting, into the public

Persistent pain is a major public health issue-estimated to affect a quarter of the world's population. Public understanding of persistent pain is based on outdated biomedical models, laden with misconceptions that are contrary to best evidence. This understanding is a barrier to effective pain management. Thus, there have been calls for public health-based interventions to address these misconceptions. Previous pain-focussed public education campaigns have targeted pain beliefs and behaviours that are thought to promote recovery, such as staying active. However, prevailing pain-related misconceptions render many of these approaches counter-intuitive, at best. Pain Science Education improves understanding of 'how pain works' and has been demonstrated to improve pain and disability outcomes. Extending Pain Science Education beyond the clinic to the wider community seems warranted. Learning from previous back pain-focussed and other public health educational campaigns could optimise the potential benefit of such a Pain Science Education campaign. Pain Science Education-grounded campaigns have been delivered in Australia and the UK and show promise, but robust evaluations are needed before any firm conclusions on their population impact can be made. Several challenges exist going forward. Not least is the need to ensure all stakeholders are involved in the development and implementation of Pain Science Education public messaging campaigns. Furthermore, it is crucial that campaigns are undertaken through a health equity lens, incorporating underrepresented communities to ensure that any intervention does not widen existing health inequalities associated with persistent pain. PERSPECTIVE: Public misconceptions about pain are a significant public health challenge and a viable intervention target to reduce the personal, social, and economic burden of persistent pain. Adaptation of Pain Science Education, which improves misconceptions in a clinical setting, into the public

OBJECTIVES: To assess the readability, credibility, and accuracy of online information on chronic pain in Australia, Mexico, and Nepal. METHODS: We assessed Google-based websites and government health websites about chronic pain for readability (using the Flesch Kincaid Readability Ease tool), credibility (using the Journal of American Medical Association [JAMA] benchmark criteria and Health on the Net Code [HONcode]), and accuracy (using 3 core concepts of pain science education: (1) pain does not mean my body is damaged; (2) thoughts, emotions, and experiences affect pain; and (3) I can retrain my overactive pain system). RESULTS: We assessed 71 Google-based websites and 15 government websites. There were no significant between-country differences in chronic pain information retrieved through Google for readability, credibility, or accuracy. Based on readability scores, the websites were "fairly difficult to read," suitable for ages 15 to 17 years or grades 10 to 12 years. For credibility, less than 30% of all websites met the full JAMA criteria, and more than 60% were not HONcode certified. For accuracy, all 3 core concepts were present in less than 30% of websites. Moreover, we found that the Australian government websites have low readability but are credible, and the majority provided all 3 core concepts in pain science education. A single Mexican government website had low readability without any core concepts but was credible. CONCLUSION: The readability, credibility, and accuracy of online information on chronic pain should be improved internationally to support facilitating better management of chronic pain.

Staphylococcus aureus (S. aureus) causes a broad range of infections and is associated with significant morbidity and mortality. S. aureus produces a diverse range of cellular and extracellular factors responsible for its invasiveness and ability to resist immune attack. In recent years, increasing resistance to last-line anti-staphylococcal antibiotics daptomycin and vancomycin has been observed. Resistant strains of S. aureus are highly efficient in invading a variety of professional and nonprofessional phagocytes and are able to survive inside host cells. Eliciting immune protection against antibiotic-resistant S. aureus infection is a global challenge, requiring both innate and adaptive immune effector mechanisms. Dendritic cells (DC), which sit at the interface between innate and adaptive immune responses, are central to the induction of immune protection against S. aureus. However, it has been observed that S. aureus has the capacity to develop further antibiotic resistance and acquire increased resistance to immunological recognition by the innate immune system. In this article, we review the strategies utilised by S. aureus to circumvent antibiotic and innate immune responses, especially the interaction between S. aureus and DC, focusing on how this relationship is perturbed with the development of antibiotic resistance.

OBJECTIVE: Identifying risk factors that contribute to the development of anorexia nervosa (AN) is critical for the implementation of early intervention strategies. Anxiety, obsessive-compulsive behavior, and immune dysfunction may be involved in the development of AN; however, their direct influence on susceptibility to the condition remains unclear. Here, we used the activity-based anorexia (ABA) model to examine whether activity, anxiety-like behavior, compulsive behavior, and circulating immune markers predict the subsequent development of pathological weight loss. METHOD: Female Sprague-Dawley rats (n = 44) underwent behavioral testing before exposure to ABA conditions after which they were separated into susceptible and resistant subpopulations. Blood was sampled before behavioral testing and after recovery from ABA to screen for proinflammatory cytokines. RESULTS: Rats that were vulnerable to pathological weight loss differed significantly from resistant rats on all key ABA parameters. While the primary measures of anxiety-like or compulsive behavior were not shown to predict vulnerability to ABA, increased locomotion and anxiety-like behavior were both associated with the extent of weight loss in susceptible but not resistant animals. Moreover, the change in expression of proinflammatory markers IL-4 and IL-6 evoked by ABA was associated with discrete vulnerability factors. Intriguingly, behavior related to risk assessment was shown to predict vulnerability to ABA. DISCUSSION: We did not find undisputable behavioral or immune predictors of susceptibility to pathological weight loss in the ABA rat model. Future research should examine the role of cognition in the development of ABA, dysfunction of which may represent an endophenotype linking anorectic, anxiety-like and compulsive behavior. PUBLIC SIGNIFICANCE: Anorexia nervosa (AN) has among the highest mortality rates of all psychiatric disorders and treatment options remain limited in their efficacy. Unders